Lesions of the vestibular organ lead to complaints of unstable vision, dizziness and imbalance. Such lesions are also accompanied by abnormalities on vestibular function testing: specifically, the vestibulo-ocular reflex (VOR) is altered, resulting in abnormal caloric responses and rotary chair testing. The VOR is a vision stabilizing reflex. In it, as the head moves, signals from the vestibular apparatus drive movements of the eyes, to keep the visual world stable. We know that small lesions of the vestibular apparatus lead to changes in the VOR. Specifically, the gain of the VOR (defined as the magnitude of the eye velocity output divided by the head velocity stimulus) may be lowered. There is a neural mechanism that adapts to changes in VOR gain. Small defects in VOR gain, such as when a spectacle prescription is worn, are rapidly corrected. However, with large changes in VOR gain, such as when the vestibular apparatus in one ear is surgically removed, the adaptive mechanism appears to fail. These patients usually have chronically low VOR gains and persistent sensations of vertigo and imbalance. There are two theoretic possibilities: the lesion could have ablated the adaptive mechanism as the VOR was disrupted, or the adaptive mechanism may have been overwhelmed by the magnitude of the lesion. The latter appears to be the case. We have tested 6 patients with persistently low VOR gains and have found that it is possible to slightly increase their VOR gains temporarily with a new method of adaptation. We have developed an immersive computer graphics environment designed for visual-vestibular interaction research. A subject wears a head mounted display that provides a wide image and blocks the view of the outside world. As the subject moves, a head position and orientation tracker measures the position of the head. The computer rendering system then shifts the scene to correspond to the new point of view. In the graphics environment the magnitude of visual scene movement relative to head movement and rate of optic flow is under software control. Our protocol for adaptation uses the computer control and uses the observation that small required changes in VOR gain are rapidly adapted to. Thus is a subject had a VOR gain of 0.4, we demagnified the scene to 0.44, thus requiring an adaptation of 10% instead of 250%. 30 minutes of exposure to successively larger increments in this paradigm proceed significant VOR gain increases at 0.32 and 0.64 Hz measured immediately after the exposure. In the proposed work here, we will test subjects after repeated exposures to successive increments in required VOR gain and determine if we can induce a persistent VOR gain change and a reduction in symptoms.